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Genetic characterization of rec-1, a mutant of Ustilago maydis defective in repair and recombination

Published online by Cambridge University Press:  14 April 2009

R. Holliday ,
R. E. Halliwell ,
M. W. Evans  and
V. Rowell
R. Holliday
Affiliation:
National Institute for Medical Research, Mill Hill, London NW7 1AA
R. E. Halliwell
Affiliation:
National Institute for Medical Research, Mill Hill, London NW7 1AA
M. W. Evans
Affiliation:
National Institute for Medical Research, Mill Hill, London NW7 1AA
V. Rowell
Affiliation:
National Institute for Medical Research, Mill Hill, London NW7 1AA
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Detailed physiological and genetic studies of haploid and diploid strains have revealed a complex phenotype for the rec-1 mutation in Ustilago maydis. The mutant is defective in the repair of damage by UV light, ionizing radiation and nitrosoguanidine. Four alleles are all recessive and have the same sensitivity to UV, suggesting the loss of a single cellular function. A significant fraction of non-viable cells is formed during growth, and in diploid strains considerable variation in colony size and morphology is seen. The spontaneous frequency of mutation is greater than in wild-type cells, but there is little, if any, enhancement by irradiation.

rec-1 also has pleiotropic effects on genetic recombination. The spontaneous level of mitotic allelic or non-allelic recombination is abnormally high, but the relative increase after irradiation is much lower than in control diploids. Allelic recombination is strongly associated with the expression of a hetozygous recessive distal marker, and it is shown that this is often due to hemizygosity rather than to homozygosity of this marker. The results indicate that allelic recombination is due to crossing over rather than gene conversion, but that the cross over is often associated with a chromatid break. rec-1 interacts with other radiation sensitive mutants, such as rec-2. Diploids homozygous for both are totally deficient in allelic recombination. In crosses between rec-1 strains meiosis is defective, with a low viability of meiotic products and frequent production of aneuploids or diploids among the survivors. The overall phenotype of rec-1 strains can best be explained in terms of the loss of a regulatory function, which leads to uncontrolled recombination during mitosis and meiosis, and the loss of a recombination repair pathway which is normally induced by agents which damage DNA.

Type
Research Article
Information
Genetics Research , Volume 27 , Issue 3 , June 1976 , pp. 413 - 453
Copyright
Copyright © Cambridge University Press 1976

References

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